Intestinal Ischemia-Reperfusion Injury Does Not Lead to Acute Central Nervous System Damage

Abstract

The detrimental effects of intestinal ischemia reperfusion (IIR) injury on secondary organs including the liver, lungs, heart, and kidney have been widely investigated in animal models. However, the effect of IIR on the central nervous system (CNS) is largely unknown. We investigated the effect of IIR on the CNS as it may be of clinical relevance to patients at high risk of neurological injury. Adult male rats underwent IIR (60 min superior mesenteric artery occlusion followed by 120 min reperfusion, n = 7) or sham operation (n = 6) under anesthesia. Following the procedure, the cerebral hemispheres were removed for histological assessment and measurement of N-acetyl-aspartate (NAA), a marker of neuronal damage, by HPLC. Blood was taken for determination of plasma S100B concentration, a measure of glial cell damage by ELISA. Data are median (range). Cerebral tissue from all animals from both groups was macroscopically and microscopically normal with no evidence of inflammation. NAA in brain homogenate was similar in the IIR group (0.2 [0.1-0.32] nmol/mg protein) and sham-operated group (0.19 [0.12-0.34], P = 0.83). Plasma S100B levels were higher in the IIR group compared to sham-operated animals but this difference was not statistically significant (1.13 [0.24-7.26] versus 0.55 [0.23-2.84] mug/l, P = 0.18). In this model, IIR injury did not produce histological CNS changes nor biochemical changes suggestive of neuronal damage. Further work is required to elucidate any functional effect of IIR injury on the CNS.